Abstract Library

Welcome to the open-access search for all ENETS abstracts presented at the Annual ENETS Conferences.

Everyone can browse the library to find basic information on abstracts. To get full access to each entry, you will be asked to log in to your myENETS account.

 

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Participants of the 2025 ENETS Conference enjoy full access to the 2025 conference digital resources through myENETS: the abstract booklet, e-posters and videos, slide decks of talks, the poster carousel, and more.

ENETS Abstract Search

#4524 SIRT7 drives the radioresistance of pancreatic neuroendocrine tumours via the DNMT1-MEN1 axis

Introduction: Pancreatic neuroendocrine tumours (PanNETs) are a rare and highly heterogeneous type of tumour in the pancreas. After failure of standard treatment, patients have poor prognoses. Radiotherapy may be a potential therapeutic modality for such patients. However, PanNETs usually exhibit a radiation “cold” tumour through unclarified mechanisms.

Conference:

Presenting Author: Jianyun J

Authors: Jiang J, Xu J, Liang Y, Chen L, Ji S,

Keywords: pancreatic neuroendocrine tumour, radio resistance, SIRT7, MEN1,

#4355 Emergence of DNA damage repair clonal haematopoiesis after peptide receptor radionuclide therapy for neuroendocrine tumours

Introduction: In neuroendocrine tumours (NETs), PRRT (Peptide Receptor Radionuclide Therapy), has shown efficacy but with significant hematologic toxicity. Clonal haematopoiesis (CHIP) is considered a risk factor for therapy-related myeloid neoplasms (t-MN).

Conference:

Presenting Author: Hadoux J

Authors: Loyaux R, Hadoux J, Oziel-Taieb S, Durand A, Bouhier Leporrier K,

Keywords: PRRT, clonal haematopoiesis, DNA Damage Repair, therapy-related myeloid neoplasm, Neuroendocrine tumour,

#4189 Pit and pitfalls of tumor mutational burden assessment in well-differentiated pancreatic neuroendocrine tumors: Two case reports from University of Verona

Introduction: The hypermutated phenotype is used as a predictive parameter for immune-checkpoint inhibitors (ICI). However, the relationship between high TMB, the underlying mutational drivers and response to ICI is still unclear.

Conference:

Presenting Author: Trevisani E

Authors: Torresan I, Reni A, Trevisani E, Borghesani M, Rossi A,

Keywords: Neuroendocrine tumor, NGS, Tumor Mutational Burden, Alkylating agent, DNA Damage Repair, Liquid biopsy,

#4182 DNA damage repair genes alterations in pancreatic neuroendocrine tumor treated with Temozolomide

Introduction: Temozolomide (TMZ), a standard therapy for pancreatic neuroendocrine tumors (pNETs), is an alkylating agent causing missense mutations and triggering cell death.

Conference:

Presenting Author: Trevisani E

Authors: Trevisani E, Reni A, Torresan I, Borghesani M, Rossi A,

Keywords: DNA Damage Repair, Tumor mutational burden, Neuroendocrine, Temozolomide,

#3928 MEN1 deficiency-induced the activation of β-Catenin-MGMT axis promotes Pancreatic Neuroendocrine Tumor growth and disrupts the response to Temozolomide

Introduction: O6-methylguanine DNA methyltransferase (MGMT) removes alkyl adducts from the guanine O6 position (O6-MG) and repairs DNA damage. High MGMT expression results in poor response to temozolomide (TMZ).

Conference:

Presenting Author: Ji S

Authors: Ji S, Xu J, Wang F, Lou X, Ye Z,

Keywords: Pancreatic neuroendocrine tumor, MGMT, MEN1, Temozolomide tolerance,